Mutation trades AIDS protection for West Nile risk

[dr. what]

linky

WASHINGTON (Reuters) - A genetic mutation that protects people from AIDS may make them more susceptible to the West Nile virus, U.S. researchers reported on Tuesday.

The study, published in the Journal of Experimental Medicine, underscores the theory that any genetic mutation that offers an advantage in one area usually has some drawback.

The mutation causes people to have blood cells lacking a receptor, a kind of molecular doorway, called CCR5. The receptor is used by the AIDS virus to dock onto immune system cells and infect them.

People who don't have CCR5 are less easily infected by the Human Immune Deficiency Virus -- although HIV can find other ways to infect them.

About 1 percent of North American whites have two copies of the mutated gene and do not produce CCR5.

Dr. Philip Murphy and colleagues at the National Institute of Allergy and Infectious Diseases noticed that mice genetically engineered to lack CCR5 receptors were especially likely to be sickened and killed by the West Nile Virus.

"We wanted to know if humans lacking CCR5 might be at greater risk of the more serious complications of WNV infection," Murphy said in a statement.

The researchers tested blood and spinal fluid samples from 395 people infected with West Nile in Arizona and Colorado in 2003 and 2004. They found that 4.5 percent of the Arizona samples were from patients who had two copies of the CCR5 mutation -- and thus did not make CCR5. Four percent of the Colorado samples showed this.

That is four times as many as would be expected, given that 1 percent of the population in general has the mutations.

Eight percent of the Colorado residents who had West Nile virus infections and identified themselves as being white had the dual mutations.

National Institutes of Health Director Dr. Elias Zerhouni said it was the first genetic risk factor identified for West Nile infection.

"While infection does not always lead to illness, the virus can sometimes cause serious problems and, according to the Centers for Disease Control and Prevention, there were 102 deaths in the United States from West Nile virus infection in 2005," he said.

West Nile virus, which is carried by mosquitoes, was first found in the United States in 1999, in a cluster of cases in New York. It has spread across the continent, including to parts of Canada and Mexico.

The findings may mean that HIV-infected patients taking certain drugs should take care to avoid being bitten. Some of these drugs block CCR5 and could make patients vulnerable to West Nile, the NIH said.

The study may also help explain why some previously healthy people are made very sick or even killed by West Nile virus.

[wautd]

Damn evolution. Can't you do anything right?

[Winston Blake]

Damn evolution. Can't you do anything right?

I think it's doing a fine job.

[Molyneux]

Damn evolution. Can't you do anything right?

I think it's doing a fine job.

So, Doctor Murphy, now you see that HIVl will always triumph because evolution is dumb.

[wolveraptor]

I think it's doing a fine job.

Is your carrier hot?

I have to wonder why American whites would develop a resistance though. HIV isn't rampant here so much as in poorer countries.

[FireNexus]

It could be a coincidence. Their may be some other virus of long ago that used the same mechanism to enter the cell. Plus HIV probably hasn't been around long enough to engender much in the way of an evolutionary response. At least in america.

[wolveraptor]

Could it be the same resistance that those people in England had to the bubonic plague (and therefore HIV, since both pathogens invade the white blood cell)? They are white, after all.

[His Divine Shadow]

I thought the CCR5 or delta32 mutation could give 100% protection against HIV if it was homozygous? or hetero, either way one form of the mutation I thought gave one immunity, this article seems to say the HIV virus has other ways...